Eupatilin attenuates TGF-β2-induced proliferation and epithelial-mesenchymal transition of retinal pigment epithelial cells

Çınar, Ayça Küpeli; Özal, Sadık Altan; Serttas, Rıza; Erdoğan, Suat

doi:10.1080/15569527.2021.1902343

Cited by 11 publications

(5 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…39 Other studies have shown that activated NF-κB is involved in the EMT of RTECs by promoting Twist1 expression and the inhibition of Twist1 expression can inhibit the proliferation and EMT of kidney fibroblasts to alleviate RIF. 19,20 The binding of IL-33 with ST2 can activate the downstream NF-κB, which then participates in the fibrosis of the heart, liver, kidney, lung, and other tissues. 40,41 In this study, we found that the p-IκBα, p-NF-κB p65, nuclear translocation of NF-κB p65, and nuclear expression of Twist1 were significantly up-regulated in the kidney tissues of UUO mice.…”

Section: Discussionmentioning

confidence: 99%

“…According to previous research methods, 19 the renal tissue was fixed with 4% paraformaldehyde and prepared into 4 μm paraffin sections. Hematoxylin-eosin (HE) staining and Masson’s trichromatic staining (KeyGEN Biotech, Nanjing, Jiangsu, China) were performed to observe the kidney histopathological changes and collagen deposition under light microscope.…”

Section: Methodsmentioning

confidence: 99%

“…18 In contrast, the inhibition of Twist1 expression can eliminate NF-κB p65-induced cell migration, invasion, and EMT characteristics. 19 Moreover, NF-κB p65 nuclear translocation increases Twist1 expression, while the knockdown or inhibition of NF-κB p65 decreases Twist1 expression. 20 These findings support that Twist1 is a downstream target gene of NF-κB, mediating NF-κB activation-induced cellular EMT.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Interleukin-33 promotes the epithelial-mesenchymal transition of renal tubular epithelial cells via the NF-κB/Twist1 signalling pathway

Zhang

et al. 2023

Eur J Inflamm

View full text Add to dashboard Cite

Objectives: Epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells (RTECs) is a pathogenic factor for renal interstitial fibrosis (RIF). Interleukin-33 (IL-33) is related to the occurrence and development of RIF, but the underlying mechanism remains unclear. Here, we investigated whether IL-33 mediates the EMT of RTECs by activating the NF-κB/Twist1 signalling pathway. Methods: In vivo, the RIF animal model induced by unilateral ureteral obstruction (UUO) was established. The effects of exogenous IL-33 and anti-IL-33 antibodies were evaluated. In vitro, the EMT of RTECs was induced by IL-33. The inhibition of the nuclear factor kappa-B (NF-κB) by the pyrrolidine dithiocarbamate (PDTC) and the knockdown of the suppression of tumorigenicity 2 (ST2) by small interference RNA were used to observe whether IL-33 mediates the EMT of RTECs through the NF-κB/Twist1 signaling pathway. Results: In vivo, exogenous IL-33 significantly aggravated UUO-induced pathological damage and collagen deposition, down-regulated E-cadherin expression, and up-regulated α-smooth muscle actin and Vimentin expressions. Moreover, exogenous IL-33 increased the levels of phospho-IκB-α (p-IκB-α) and phospho-NF-κB p65 (p-NF-κB p65), NF-κB p65 nuclear translocation, and Twist1 nuclear expression. However, these effects were reversed by the anti-IL-33 antibody. In vitro , the increases in the levels of p-IκB-α, p-NF-κB p65, NF-κB p65 nuclear translocation, and Twist1 nuclear expression induced by IL-33 were inhibited by the knockdown of PDTC or ST2. IL-33-mediated EMT of RTECs was also significantly reversed. However, NF-κB inhibitor PDTC had no significant effect on ST2 expression. Conclusions: The IL-33/ST2 axis may up-regulate the expression of Twist1 through the NF-κB signalling pathway, thereby inducing the EMT of RTECs and leading to RIF.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Interleukin-33 promotes the epithelial-mesenchymal transition of renal tubular epithelial cells via the NF-κB/Twist1 signalling pathway

Zhang

et al. 2023

Eur J Inflamm

View full text Add to dashboard Cite

show abstract

“…(2) Eupatilin: Eupatilin, a lipophilic flavonoid isolated from ARTEMISIAE ARGYI FOLIUM, is a PPARα agonist with anti-apoptotic, anti-oxidant and anti-inflammatory effects ( 286 – 288 ). Eupatilin may inhibit pro-inflammatory mediators including nitrite, PGE2, TNF-α and IL-6 in activated microglia in vitro and in vivo to combat focal cerebral ischemia.…”

Section: Modulatory Effects Of Natural Botanical Components On Microg...mentioning

confidence: 99%

The mechanism of microglia-mediated immune inflammation in ischemic stroke and the role of natural botanical components in regulating microglia: A review

et al. 2023

View full text Add to dashboard Cite

Ischemic stroke (IS) is one of the most fatal diseases. Neuroimmunity, inflammation, and oxidative stress play important roles in various complex mechanisms of IS. In particular, the early proinflammatory response resulting from the overactivation of resident microglia and the infiltration of circulating monocytes and macrophages in the brain after cerebral ischemia leads to secondary brain injury. Microglia are innate immune cells in the brain that constantly monitor the brain microenvironment under normal conditions. Once ischemia occurs, microglia are activated to produce dual effects of neurotoxicity and neuroprotection, and the balance of the two effects determines the fate of damaged neurons. The activation of microglia is defined as the classical activation (M1 type) or alternative activation (M2 type). M1 type microglia secrete pro-inflammatory cytokines and neurotoxic mediators to exacerbate neuronal damage, while M2 type microglia promote a repairing anti-inflammatory response. Fine regulation of M1/M2 microglial activation to minimize damage and maximize protection has important therapeutic value. This review focuses on the interaction between M1/M2 microglia and other immune cells involved in the regulation of IS phenotypic characteristics, and the mechanism of natural plant components regulating microglia after IS, providing novel candidate drugs for regulating microglial balance and IS drug development.

show abstract

“…Recently, transcription factors that promote EMT, such as Snail, Zeb1, Zeb2, AP-1, Sp1, and LEF1/TCF, have been found to interact as cofactors for Smads ( 61 ). TGF-β2 increases the expression of the transcription factors Twist, Snail, slug, and Zeb1 in RPE, followed by EMT ( 51 , 62 ). The retinoic acid signaling pathway mediated by the retinoic acid receptor (RAR), which is a nuclear receptor, also affects the TGF-β/Smad signaling pathway through binding of RAR to Smad ( 63 ).…”

Section: Subsections Relevant For the Subjectmentioning

confidence: 99%

Molecular mechanisms of TGFβ-mediated EMT of retinal pigment epithelium in subretinal fibrosis of age-related macular degeneration

Higashijima

Hasegawa²,

Yoshimoto³

et al. 2023

Front. Ophthalmol.

View full text Add to dashboard Cite

Age-related macular degeneration (AMD) is one of the leading causes of blindness in the elderly, affecting the macula of the retina and resulting in vision loss. There are two types of AMD, wet and dry, both of which cause visual impairment. Wet AMD is called neovascular AMD (nAMD) and is characterized by the formation of choroidal neovascular vessels (CNVs) in the macula. nAMD can be treated with intravitreal injections of vascular endothelial growth factor (VEGF) inhibitors, which help improve vision. However, approximately half the patients do not achieve satisfactory results. Subretinal fibrosis often develops late in nAMD, leading to irreversible photoreceptor degeneration and contributing to visual loss. Currently, no treatment exists for subretinal fibrosis, and the molecular mechanisms of fibrous tissue formation following neovascular lesions remain unclear. In this review, we describe the clinical features and molecular mechanisms of macular fibrosis secondary to nAMD. Myofibroblasts play an essential role in the development of fibrosis. This review summarizes the latest findings on the clinical features and cellular and molecular mechanisms of the pathogenesis of subretinal fibrosis in nAMD and discusses the potential therapeutic strategies to control subretinal fibrosis in the future.

show abstract

Eupatilin attenuates TGF-β2-induced proliferation and epithelial-mesenchymal transition of retinal pigment epithelial cells

Cited by 11 publications

References 41 publications

Interleukin-33 promotes the epithelial-mesenchymal transition of renal tubular epithelial cells via the NF-κB/Twist1 signalling pathway

Interleukin-33 promotes the epithelial-mesenchymal transition of renal tubular epithelial cells via the NF-κB/Twist1 signalling pathway

The mechanism of microglia-mediated immune inflammation in ischemic stroke and the role of natural botanical components in regulating microglia: A review

Molecular mechanisms of TGFβ-mediated EMT of retinal pigment epithelium in subretinal fibrosis of age-related macular degeneration

Contact Info

Product

Resources

About